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Biomedical subjects

J Butany

Publications and source records attributed to J Butany.

At least 55 records · Page 3Linked to original sources
PubMed1993

The vascular pathology of human hepatic allografts.

Studies of hepatic transplant vasculopathy (TV) have described arterial lesions in selected cases but have not sought to establish the relative prevalence of various arterial and venous lesions. We examined 20 unselected liver allografts and 12 controls to establish the spectrum and distribution of transplant-related arterial and venous lesions. Sections of 1,175 arteries and 936 portal and hepatic veins were reviewed and several histologic parameters were tabulated. Fibrotic (18 cases: 184 arteries and 17 veins) and cellular (10 cases: 353 arteries and 33 veins) lesions were seen. Three allografts had evidence of severe TV with abundant foam cell, myointimal, and mixed fibrocellular lesions in the intima of arteries. These three grafts also had foam cells in portal veins. Allografts with TV had more stenotic arteries (P < .05) and more intimal cellular proliferation (P < .05) compared with non-TV allografts and with controls. Foam cells often demonstrated immunoperoxidase staining for actin, lysozyme, or UCHL-1. Two of the TV cases had marked paucity of bile ducts and required retransplantation.

Adult↗
PubMed1993

Serological response to Ureaplasma urealyticum in the neonate.

A serovar-specific antibody response to Ureaplasma urealyticum was observed in stillborns, neonates, and mothers by means of the modified metabolic inhibition test. Elevated levels of ureaplasma antibody were found in cases of stillbirth and neonatal respiratory disease. There was a higher risk of mortality among neonates with respiratory disease who had elevated levels of ureaplasma antibody. IgG and IgM serovar-specific antibody responses to U. urealyticum serovars were confirmed by the immunoperoxidase and immunofluorescence assays. In contrast to ELISA-based assays that use soluble membrane proteins as antigen, these three assays use whole intact cells. These observations suggest that the serovar-specific antibody response may be associated with the ureaplasma extramembranous carbohydrate (lypoglycan) coat, which comes off during centrifugation. With the immunoperoxidase assay, a heel-prick blood sample (20 microL) can be screened for 16 IgM or IgG + IgM + IgA (combined) responses in 4 hours. The predictive value of IgM antibody for U. urealyticum infection and other mycoplasma infections and for the risk of stillbirth and development of chronic lung disease should now be assessed.

Antibodies, Bacterial↗
PubMed1992

Production and reversibility of right ventricular hypertrophy and right heart failure in dogs.

Combined heart-lung transplantation has been used for end-stage primary pulmonary hypertension. Experience with single-lung transplantation for other conditions suggested that associated severe right ventricular dysfunction resulting from increased afterload would recover after placement of a satisfactory lung allograft. Early experience with the application of single-lung transplantation for pulmonary hypertension supports this contention. We devised a reversible canine model of chronic progressive pressure-overloaded right heart failure by pulmonary artery banding to study the echocardiographic, hemodynamic, and pathological reversibility of the failing right heart. Clinical right heart failure was defined as the development of ascites and pleural effusions. Right heart failure developed in 23 dogs 67 to 348 days after banding, and they were divided into two groups to determine its early and long-term effects. Group 1 dogs (n = 11) were either sacrificed immediately after the onset of right heart failure (n = 5) or unbanded (n = 6); group 2 dogs (n = 12) were maintained in right heart failure for 3 months and then either sacrificed (n = 6) or unbanded. Unbanded dogs in both groups were observed for 4 additional months before sacrifice. A control group of 6 normal dogs was sacrificed for pathological comparisons. After unbanding, the right ventricular systolic pressure fell from 97 +/- 17 mm Hg (group 1) and 88 +/- 31 mm Hg (group 2) to 44 +/- 11 mm Hg and 47 +/- 13 mm Hg, respectively. Despite this persistent gradient across the pulmonary artery, echocardiographic and hemodynamic measures of right ventricular function returned to normal, albeit more slowly in the group 2 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Morphologic findings and causes of failure in 24 explanted Ionescu-Shiley low-profile pericardial heart valves.

From 1981 to 1987 just over 608 Ionescu-Shiley low-profile bovine pericardial bioprostheses were implanted at the Toronto Hospital. Twenty-four prostheses (11 aortic and 13 mitral) were surgically explanted from 1988 to 1990 from 20 adults (10 men and 10 women). Prosthesis failure was caused by primary tissue failure in 17 valves or by other mechanisms in seven valves. Variable degrees of tissue failure were also seen in four of the seven valves from the latter group. Primary tissue failure was characterized by fluid insudation between collagen bundles, para stent post tears (alignment stitch related, 20 valves), cusp perforation with prolapse, and calcification. The earliest cusp tears occurred at 28 months. Calcification (10 of 24 cases) was minimal in seven of 10 valves (occurring primarily at the margins of the torn cusp), moderate in two, and severe in one. Tissue overgrowth (pannus) was seen in all but three prostheses. Like its predecessor, the Ionescu-Shiley standard pericardial valve, this prosthesis failed at 2 to 5 years largely due to design-related (alignment stitch) causes and tissue degeneration. Calcification was less prominent, while tissue overgrowth (pannus) was more marked.

Adult↗
PubMed1992

Morphology of graft arteriosclerosis in cardiac transplant recipients.

The morphologic features of graft arteriosclerosis (GA) and other vascular lesions were semiquantitatively evaluated. Five failed cardiac allografts attributable to GA and five other allografts were obtained from nine autopsies and one surgical explanation. The subjects, aged 4.5 to 67 years, had a mean allograft survival of 735 +/- 184 days. A total of 1,174 arterial and 754 venous cross-sections were reviewed. Intimal fibrosis (nine cases, 254 arteries, and 118 veins), fibrofatty plaques (eight cases and 35 arteries), and cellular intima thickening and concentric foam cell lesions (eight cases, 326 arteries, and 20 veins) were seen. Cellular lesions contained T lymphocytes, monocytes, and cells of smooth muscle cell origin detected by staining using the immunoperoxidase technique. Allografts with severe GA had a greater luminal stenosis in epicardial arteries (P less than .05), greater cellular proliferation in large mural arterial lesions (P less than .004), and more foam cell lesions in both arteries (P less than .06) and veins (P less than .03) than other allografts. Medical fibrosis and thinning were present in six allografts. Severity of acute rejection (P less than .01) was correlated with the presence of GA. The morphology and distribution of GA is heterogeneous, with evidence supporting an immune-mediated pathogenesis.

Adult↗
PubMed1992

Verapamil ameliorates the clinical and pathological course of murine myocarditis.

The effects of the calcium channel blocking agent, verapamil, were studied in a murine model of viral myocarditis. Three groups of 8-wk-old DBA/2 mice (n = 25 each) were inoculated with 10 plaque-forming units of encephalomyocarditis virus and randomized to three treatment regimens. Group 1 mice received verapamil intraperitoneally (5 mg/kg per d) for 7 d before infection, followed by verapamil orally (mean dose of 3.5 mg/mouse per d) in drinking water during infection. Group 2 mice received only verapamil orally starting on day 4 after infection, coincident with peak viremia. Group 3 (infected control) received no verapamil in regular drinking water after viral inoculation. Additional control animals were studied in group 4 (n = 21), consisting of uninfected control animals receiving intraperitoneal and oral verapamil at doses identical to group 1, and in group 5 (n = 21), consisting of uninfected and untreated controls. Animals were randomly killed from each group (n = 7) at 7, 14, and 28 d after infection. Routine histology was performed blindly on an apical slice of each heart and semi-quantitatively graded for inflammation, necrosis, calcification, and fibrosis on a scale of 0-4. Digital planimetry was performed to measure the absolute and relative areas of inflammation and necrosis. The pretreated animals in group 1 showed marked reduction in inflammation and necrosis (score of 3.7 +/- 1.4 vs. 8.7 +/- 2.0 in group 3 on day 14, P < 0.05) and were indistinguishable from the posttreated group 2 mice (score of 4.0 +/- 1.5 vs. 8.7 +/- 2.0 in group 3 on day 14, P < 0.05). All the uninfected control animals (groups 4 and 5) showed no myocardial lesions whether treated with verapamil or not. Quantitative planimetry confirmed decreased inflammation and necrosis (2.0 +/- 3.3% in group 1 and 3.5 +/- 3.1% in group 2 vs. 21.9 +/- 22.6% in group 3 on day 14). Untreated infected hearts injected with liquid silicone rubber exhibited extensive areas of focal microvascular constriction and microaneurysm formation; verapamil treatment in either group 1 or 2 completely abolished these abnormalities, resembling uninfected controls in groups 4 or 5. We conclude that verapamil, whether given before infection or after peak viremia in an encephalomyocarditis model of murine myocarditis, significantly reduces the microvascular changes and myocardial necrosis, fibrosis, and calcification leading to cardiomyopathy. This suggests the potentially important role of calcium and microvascular spasm in the pathogenesis of viral myocarditis leading to dilated cardiomyopathy, and may have future therapeutic implications.

Animals↗
PubMed1992

Altered distribution of desmin filaments in hypertrophic cardiomyopathy: an immunohistochemical study.

Hypertrophic cardiomyopathy (HCM) is characterized by myofiber hypertrophy and disarray. Intermediate filaments play an important role in maintaining of normal cell shape. Desmin filaments have been detected in adult cardiomyocytes, and vimentin and keratin filaments in cardiomyocytes during embryonic development. The pattern of arrangement of intermediate filaments in HCM has not been reported. We examined the distribution of intermediate filaments in formalin-fixed tissue sections of the disarrayed myofibers from 10 hearts with HCM using an immunohistochemical technique and antibodies to desmin, vimentin, and high and low molecular weight keratins. The controls consisted of subaortic tissue from surgically explanted hearts of patients with ischemic heart disease. In the ischemic hearts, desmin was detected in the Z bands and intercalated disks. In all HCM cases, three patterns of staining for desmin were noted: (a) individual myocytes showing a parallel arrangement along Z bands; (b) focal myofibers with decreased or complete loss of labeling of Z bands; and (c) individual myocytes with intense granular cytoplasmic staining especially in disarrayed myofibers. No staining for vimentin or keratins was noted in the cardiomyocytes from either the HCM or ischemic cases. The altered arrangement of desmin filaments in the disarrayed cardiac muscle fibers may play a role in the altered contractility that occurs in patients with HCM.

Adult↗
PubMed1992

Fatal esophageal-arterial fistula 17 years following tetralogy of Fallot repair.

Blalock-Taussig shunts (subclavian to pulmonary anastomoses) have remained the most effective palliation in cyanotic heart disease. Late complications are rare but can be devastating. The case of a 26-year-old female with tetralogy and an original Blalock shunt constructed at age four years is reported. Despite subsequent primary repair of the tetralogy and presumed ligation of the Blalock shunt, the patient succumbed to a fatal hemorrhage due to esophageal-arterial fistula involving the Blalock shunt. The circumstances leading to this dramatic outcome are outlined and discussed. It is important for cardiologists caring for congenital heart disease patients to be aware of the late complications of congenital heart surgery, and carry out the proper follow-up investigations.

Adult↗
PubMed1992

Right ventricular dysplasia: morphological findings in 13 cases.

OBJECTIVE: To characterize the pathological features of right ventricular dysplasia (RVD). DESIGN: Retrospective morphological case study. SETTING: Three referral-based university medical centres. PATIENTS: Thirteen subjects (one female) aged 16 to 55 years including 10 necropsy hearts from sudden deaths out of hospital, one explant heart and two partial right ventricular resections from patients with intractable ventricular tachycardia. MAIN RESULTS: Most hearts showed hypertrophy and localized or generalized dilatation of the right ventricle. Transillumination revealed myocardial thinning of variable configuration usually conforming to regions of dilatation. Common sites of involvement were apex, infundibular region and posterobasal wall. Histologically, focal or extensive segments of right ventricular myocardium were absent or replaced. Three patterns were found: right ventricle markedly thinned, epicardium and endocardium contiguous, virtually no intervening tissue; wall normal thickness or thinned, myocardium almost totally replaced by fat; and wall normal or thin, myocardium largely replaced by fat with scattered residual myocardial cells and fibrous tissue (the predominant pattern). Endocardial fibrosis was present in eight cases and focal mononuclear cell infiltrates in 10. Electron microscopy in two cases showed nonspecific findings. CONCLUSIONS: RVD has gross and microscopic features which permit its recognition. While a majority of cases are likely congenital (genetic or acquired in utero), the possibility of postnatally acquired conditions (inflammatory, toxic, ischemic) inducing RVD must be explored. The incidence and importance of RVD as a cause of sudden death can only be assessed by continued systematic and detailed studies of patients with recurrent ventricular tachycardia and of hearts, especially from sudden death victims. Although uncommon, RVD should be considered in the differential diagnosis of arrhythmia and sudden death by both clinicians and pathologists.

Adolescent↗
PubMed1991

Pathologic fibrosis and matrix connective tissue in the subaortic myocardium of patients with hypertrophic cardiomyopathy.

To evaluate scar-type and matrix connective tissue and to assess their role in the diastolic dysfunction of hypertrophic cardiomyopathy, surgically resected subaortic myectomy specimens and several autopsy hearts from patients with hypertrophic cardiomyopathy were studied. Eighteen specimens were differentially stained by a newly developed method that precisely determines relative collagen content; these tissues were compared with postmortem hypertrophied and normal control subaortic specimens. Quantitation revealed a 72% higher level (36.5 vs. 22.1 micrograms collagen/mg protein) of stainable collagen in the hearts with hypertrophic cardiomyopathy than in hypertrophied control hearts. The endocardial plaque was quantitated morphometrically, and it constituted only 4.6 +/- 1.7% of the total increased collagen content in the cardiomyopathy specimens. For the matrix studies, the cardiomyopathy specimens were stained by a silver impregnation technique that identifies connective tissue elements not normally visible with routine histologic methods. There was a marked increase in content of all matrix components, both in areas of pathologic scarring and in "normal" zones. Whorls of matrix connective tissue were noted in regions of myocyte whorls, as well as independent of them. Thus, these studies revealed a striking increase of both scar-type and matrix connective tissue in hypertrophic cardiomyopathy. The extensive scarring and the pronounced interstitial and intercellular matrix connective tissue may contribute to the increased ventricular chamber stiffness and impaired relaxation in this disease.

Cardiomyopathy, Hypertrophic↗
PubMed1990

Intraabdominal hemorrhage as a result of segmental mediolytic arteritis of an omental artery: case report.

This article describes the fifth reported case of segmental mediolytic arteritis and the second in a survivor. The patient had intraabdominal bleeding as a result of a ruptured omental artery. The pathologic and arteriographic findings are described. The pathology is characterized by segmental disruption of the medial smooth muscle cells and the initiation of mediolysis. Mediolysis is associated with marked segmental thinning of the vessel wall, often with only the adventitia intact. Fibrin is deposited at the adventitial and medial surfaces, and hemorrhage into the media may occur. As in this reported case, lysis of the adventitia leads to sudden, often catastrophic intraabdominal hemorrhage. Little associated adventitial inflammation occurred. Segmental mediolytic arteritis seems to involve the intra-abdominal muscular arteries in elderly patients with nonspecific abdominal symptoms. An angiogram showed patchy areas of narrowing involving ileal, gastroduodenal, and renal arteries that correlated with the pathologic findings observed in the excised omental arteries.

Abdomen↗
PubMed1990

Are the kinetics of technetium-99m methoxyisobutyl isonitrile affected by cell metabolism and viability?

To investigate the role of cell viability and metabolism on the myocardial kinetics of a new tracer, technetium-99m-methoxyisobutyl isonitrile (Tc-99m-MIBI), 250 microCi/l Tc-99m-MIBI was infused in isolated rat hearts under constant flow conditions. The hearts were studied after inducing irreversible damage by cytochrome c oxidase inhibitor sodium cyanide (n = 8) or sarcolemmal membrane detergent Triton X-100 (n = 8). The control hearts (n = 6) received no toxins. Mean Tc-99m-MIBI peak accumulation activity was significantly reduced after cyanide (51.1 +/- 44.2% of control, p less than 0.01) and Triton (13.8 +/- 2.7% of control, p less than 0.001) administration. Kinetic studies also showed marked reduction in accumulation rates and marked increase in clearance rates for cyanide (p less than 0.01) and Triton (p less than 0.01) groups compared with controls. Potential changes in regional flow distribution were assessed using microspheres. When peak accumulation activity was corrected for these changes, there remained significant differences between the groups. In the cyanide and Triton groups, irreversible cell injury was confirmed by creatine kinase and lactate dehydrogenase release, triphenyl tetrazolium chloride staining, and electron microscopy. All the cells were viable in the control group. We conclude that the accumulation and clearance kinetics of Tc-99m-MIBI are significantly affected by cell viability. Tc-99m-MIBI kinetics appear to be dependent on sarcolemmal integrity and to a lesser extent on aerobic metabolism.

Animals↗
PubMed1990

Fatal left ventricular perforation following balloon mitral valvuloplasty.

Left ventricular perforation following a balloon mitral valvuloplasty is a rare complication. This paper reports morphological findings in such a case that was fatal. Cardiac tamponade was suspected clinically, but could not be confirmed or treated because of extensive anterior pericardial adhesions related to a previous closed mitral commissurotomy.

Balloon Occlusion↗
PubMed1990

Myocarditis and myocardial hemorrhage associated with thrombotic thrombocytopenic purpura.

Four patients with thrombotic thrombocytopenic purpura (TTP) developed severe cardiac dysfunction. Endomyocardial biopsy in one patient demonstrated focal myocarditis associated with platelet microthrombi. Cardiac function and TTP improved after plasmapheresis therapy in this as well as in two other patients. A fourth patient died owing to extensive intramyocardial confluent hemorrhages. Cardiac involvement in TTP may be due to microvascular thrombosis, hemorrhage, or myocarditis. Severe myocardial dysfunction may improve with treatment aimed at the underlying hematologic disorder.

Adult↗
PubMed1988

Five-year follow-up of Hancock pericardial valves: management of premature failure.

The durability and function of bovine pericardial valves are dependent upon design, preservation, patient factors (age, sex), and site of valve implantation. In 1983, a shelf recall of all Hancock bovine pericardial valves (HPV) was instituted by the manufacturer. This report represents the results of an organized 5-year follow-up in a hospital Prosthetic Valve Registry of 129 HPV implanted in 122 patients (79 males, 43 females) between May 1982 and April 1985 using echo Doppler and careful clinical evaluation. Mean age was 56 +/- 15 years. There were 81 AVR, 33 MVR, 7 DVR, and 1 TVR. Concomitant coronary bypass was performed in 38 patients (31%). Surgery was on a redo basis in 25 patients (20%), urgent in 14 (11%), and for SBE in 8 patients (7%). There were seven hospital deaths (5.7%). Mean follow-up was 44 months (maximum 66 months) for 114 patients (99% complete), representing 417 patient years. There have been 20 late deaths (18%), of which 7 were directly valve related. Linearized frequency of major events (per pt-yr) was: thromboembolism, 1.6%; anticoagulant related hemorrhage, 0.8% (1 late death); prosthetic valve endocarditis 1.3%; primary tissue failure, 5.8%. Patient symptomatology was a more accurate predictor of bioprosthetic failure requiring reoperation than echo Doppler studies, which were completed in 74 of 97 patients examined during scheduled follow-up visits. Twenty-four of the 96 patients (25%) have required re-replacement at a mean interval of 44 months (27-59 months) from initial implantation. This was due to vertical shear starting at the top of the strut anchoring commissural attachments in every case.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Clinical results of pericardial xenograft valves: the Ionescu-Shiley and Hancock valves.

Between 1979 and 1985, 552 Ionescu-Shiley valves were implanted in 511 patients. The Hancock valve was implanted in 122 patients (129 valves) between 1982 and 1983. Sixty percent of procedures were isolated aortic valve replacements. In the Ionescu series, 59% of these were 19 or 21 mm valves while only 15% of the Hancock valves were of this size. For isolated mitral valve replacement, 76% of Ionescu-Shiley valves were 25 to 27 mm, compared to 36% of the Hancock valves. Patient age, sex, prior operations, concomitant surgery (usually coronary bypass), operative mortality and late deaths were similar for both valves. A mean follow-up of 38 months was obtained for each valve population (99% complete) representing a cumulative 1497 patient-years for the Ionescu-Shiley valve and 375.4 patient-years for the Hancock valve. Actuarial survival for the former was 73 +/- 4% at 72 months, and 65 +/- 14% for Hancock valves at 60 months. The frequency of major events during follow-up (thromboembolism, anticoagulant related hemorrhage, bland perivalvular leak and prosthetic valve endocarditis) were similar, but the frequency of primary tissue valve failure was markedly different for the two valves (1.1% per patient-year for Ionescu-Shiley valves and 5.9% for the Hancock valve). The mean interval to replacement of an Ionescu mitral prosthesis was significantly shorter (23.4 months) than for replacement of an aortic prosthesis (42 months) while the mean interval to replacement of an Ionescu aortic and/or a Hancock aortic or mitral were all similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗